Fter 3 days of AMV with diaphragm muscle activation between 30 and 80 of spontaneous breathing. Whether diaphragm muscle activation between 0 and 30 is effective to maintain Po remains unknown. Data obtained from [41]: n = 6 for the control and controlled mechanical ventilation (CMV) groups; n = 5 for the AMV group.The lack of IMT benefits may be due to the small PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/27663262 sample size [44]. It is also conceivable that the magnitude of the stimulus for IMT, as a percentage of the PImax, in the critically ill patients (that is, the threshold load applied, and/or session frequency and duration) was inadequate to elicit a physiological training effect. Measurements of PImax in the critically ill patients are challenging and highly dependent on patient volitional effort and the methods of measurement. Alternatively, in view of the complexity of the underlying mechanisms of CMV-induced diaphragmatic dysfunction, diaphragm muscle conditioning alone is inadequate, and pharmacological intervention may be required to mitigate diaphragm muscle weakness.Mechanisms of the interactive effects of mechanical ventilation and short-term high-dose corticosteroid on diaphragm muscle dysfunctionShort-term high-dose corticosteroid has been administered for its anti-inflammatory and immunosuppressive effects in critically ill patients [9,45]; the treatment might be responsible for the development of acquired paresis in the critically ill patient, referred to as critical-illness myopathyPage 6 of(page number not for citation purposes)Evidence of methylprednisolone-induced diaphragmatic dysfunction in humans and a potential approach to preventionAs with CMV, the extent to which acute, high-dose MP could contribute to diaphragm muscle weakness in critically ill patients is difficult to determine. This difficulty stems from the many confounding factors in these patients, and from the lack of data on functional or structural alterations in humans. Indirect data, however, suggest that such interaction may occur in critically ill patients [46].Available online http://ccforum.com/content/13/5/FigureCross-sectional areas of diaphragm muscle. Cross-sections of diaphragm muscle from biopsy specimens of a representative organ donor subject ((a), (c), (e)) and from a control ((b), (d), (f)). (a) and (b) Muscle fibers in the organ donor subject are in general smaller than those in the control diaphragm. No inflammatory infiltrate or necrosis is seen. Stained with hematoxylin and eosin. (c) and (d) Stained with antibody specific for slow myosin, heavy chain. (e) and (f) Stained with antibody specific for fast myosin, heavy chain. In (c) to (f), fibers reacting with the antibody appear orange ed, whereas fibers not reacting with the antibody appear black; open circle, slow-twitch fibers; open square, fast-twitch fibers. In addition, all fibers in each section are outlined by an antibody reactive to laminin. Reproduced with permission from [8]. Copyright ?2008 Massachusetts Medical Trichostatin A web Society. All rights reserved.First, in a prospective study of critically ill patients receiving mechanical ventilation for longer than 7 days, De Jonghe and colleagues reported a strong association between the occurrence of neuromyopathy and the administration of corticosteroids [46]. Second, in patients with acute spinal cord injury, the administration of recommended high-dose MP for 48 hours resulted in paraspinal muscle necrosis and type II fiber atrophy in four out of five patients [9]. Three of the.
